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While the role of activated T cells in the osteoporosis driven by inflammatory conditions and infection has been well documented, only recently has the role of T cells in the bone destruction associated with estrogen deficiency begun to be appreciated. <jats:italic>In vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic> models of postmenopausal osteoporosis demonstrate that estrogen deficiency leads to an increase in the adaptive immune function that culminates in an increased production of tumor necrosis factor \u03b1 (TNF) by activated T cells. TNF increases osteoclast (OC) formation and bone resorption both directly and by augmenting the sensitivity of maturing OCs to the essential osteoclastogenic factor receptor activator of nuclear factor \u03baB ligand. The activation and expansion of TNF\u2010producing T cells are key steps in estrogen deficiency\u2010driven bone loss and are regulated by multiple interacting cytokines including transforming growth factor\u2010\u03b2, interleukin\u20107, and interferon\u2010\u03b3, as well as by the process of antigen presentation. Herein, we review the experimental evidence that suggests estrogen prevents bone loss by regulating T\u2010cell function and immune cell bone interactions.<\/jats:p>","DOI":"10.1111\/j.0105-2896.2005.00324.x","type":"journal-article","created":{"date-parts":[[2006,5,11]],"date-time":"2006-05-11T12:17:12Z","timestamp":1147349832000},"page":"154-168","source":"Crossref","is-referenced-by-count":148,"title":["The role of T lymphocytes in bone metabolism"],"prefix":"10.1111","volume":"208","author":[{"given":"M. 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